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关于肝硬化时门脉高压的形成和持续,长期存在2种不同的学说:“后向血流”学说和“前向血流”学说。前者认为门脉高压的形成是由于门脉血管阻力增加所致,这种阻力主要来自肝窦与肝内血管;后者认为肝硬化门脉高压的始动因子是门脉阻力增加,侧支循环的形成可缓解门脉压力,但随之而来的高动力循环增加了门脉血流量,导致了门脉高压的持续存在。近年来不少学者研究证实了内毒素(LPS)、一氧化氮(NO)在这两种学说中起着重要作用,与门脉高压的持续存在有着重大关系,
About the formation and persistence of portal hypertension in cirrhosis, there are two different kinds of doctrine that exist for a long time: the doctrine of “backward flow” and the theory of “forward flow”. The former believes that the formation of portal hypertension is due to an increase in portal vascular resistance, which mainly comes from the sinusoids and intrahepatic blood vessels; the latter that the initiating factor of cirrhosis and portal hypertension is increased portal pressure, collateral circulation The formation of portal pressure can be alleviated, but the consequent high power cycle increases portal blood flow, resulting in the persistence of portal hypertension. In recent years, many scholars have confirmed that endotoxin (LPS) and nitric oxide (NO) play an important role in these two theories and have a significant relationship with the persistence of portal hypertension.